Muscle regeneration after damage or during myopathies requires a fine cooperation between myoblast proliferation and myogenic differentiation. A growing body of evidence suggests that microRNAs play critical roles in myocyte proliferation and differentiation transcriptionally. However, the molecular mechanisms underlying the orchestration are not fully understood. Here, we showed that miR-130b is able to repress myoblast proliferation and promote myogenic differentiation via targeting Sp1 transcription factor. Importantly, overexpression of miR-130b is capable of improving the recovery of damaged muscle in a freeze injury model. Moreover, miR-130b expression is declined in the muscle of muscular dystrophy patients. Thus, these results indicated that miR-130b may play a role in skeletal muscle regeneration and myopathy progression. Together, our findings suggest that the miR-130b/Sp1 axis may serve as a potential therapeutic target for the treatment of patients with muscle damage or severe myopathies.

中文翻译：

---

miR-130b 通过靶向 Sp1 抑制心肌细胞增殖并促进分化。


损伤后或肌病期间的肌肉再生需要成肌细胞增殖和肌原性分化之间的良好配合。越来越多的证据表明 microRNA 在心肌细胞增殖和转录分化中发挥着关键作用。然而，编排背后的分子机制尚未完全了解。在这里，我们发现 miR-130b 能够通过靶向 Sp1 转录因子来抑制成肌细胞增殖并促进肌原性分化。重要的是，miR-130b 的过度表达能够改善冷冻损伤模型中受损肌肉的恢复。此外，肌营养不良症患者的肌肉中 miR-130b 表达下降。因此，这些结果表明 miR-130b 可能在骨骼肌再生和肌病进展中发挥作用。总之，我们的研究结果表明 miR-130b/Sp1 轴可能作为治疗肌肉损伤或严重肌病患者的潜在治疗靶点。